Correlation between glomerular filtration rate and urinary N acetyl-beta-D glucosaminidase in children with persistent proteinuria in chronic glomerular disease.
10.3345/kjp.2012.55.4.136
- Author:
Jeong Deok HONG
1
;
In Seok LIM
Author Information
1. Department of Pediatrics, Chung-Ang University College of Medicine, Seoul, Korea. inseok@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Proteinuria;
Glomerular filtration rate;
N acetyl-beta-D glucosaminidase
- MeSH:
Child;
Creatinine;
Cystatin C;
Glomerular Basement Membrane;
Glomerular Filtration Rate;
Glomerulonephritis;
Glomerulonephritis, IGA;
Glomerulosclerosis, Focal Segmental;
Hexosaminidases;
Humans;
Nephritis;
Proteinuria;
Renal Insufficiency, Chronic;
Urinalysis
- From:Korean Journal of Pediatrics
2012;55(4):136-142
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Urinary excretion of N acetyl-beta-D glucosaminidase (NAG) and beta2-microglobulin (beta2-M) was increased in the presence of proximal tubular damage. Based on these urinary materials, we investigated the ability of expecting renal function in chronic glomerular diseases. In this study, we evaluated the relationship between glomerular filtration rate (GFR) urinary NAG, and urinary beta2-M. METHODS: We evaluated 52 children with chronic kidney disease at the Chung-Ang University Hospital between January 2003 and August 2009. We investigated the 24-hour urinalysis and hematologic values in all 52 patients. Serum creatinine, creatinine clearance (Ccr), serum cystatin C, urinary beta2-M and urinary NAG were measured. RESULTS: Out of 52 patients, there were 13 children with minimal change in disease, 3 children with focal segmental glomerulosclerosis, 17 children with immunoglobulin A nephropathy, 15 children with Henoch-Schonlein purpua nephritis, 3 children with poststreptococcal glomerulonephritis, and 1 child with thin glomerular basement membrane disease. In these patients, there were significant correlation between the Ccr and urinary NAG (r=-0.817; P<0.01), and between the GFR (as determined by Schwartz method) and urinary NAG (r=-0.821; P<0.01). In addition, there was a significant correlation between the GFR (as determined by Bokencamp method) and urinary NAG (r=-0.858; P<0.01). CONCLUSION: In our study, there was a significant correlation between the GFR and urinary NAG, but there was no correlation between the GFR and urinary beta2-M, suggesting that the GFR can be predicted by urinary NAG in patients with chronic glomerular disease.
